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成年猫对持续性低氧的双相通气反应起源于中枢。

Biphasic ventilatory response of adult cats to sustained hypoxia has central origin.

作者信息

Vizek M, Pickett C K, Weil J V

机构信息

Cardiovascular Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver 80262.

出版信息

J Appl Physiol (1985). 1987 Oct;63(4):1658-64. doi: 10.1152/jappl.1987.63.4.1658.

Abstract

Hypoxia stimulates ventilation, but when it is sustained, a decrease in the response is often seen. The mechanism of this depression or "roll off" is unclear. In this study we attempted to localize the responsible mechanism at one of three possible sites: the carotid bodies, the central nervous system (CNS), or the ventilatory apparatus. The ventilatory response to sustained hypoxia (PETO2, 40-50 Torr) was tested in 5 awake and 14 anesthetized adult cats. The roll off was found in both anesthetized and awake cats. Isocapnic hypoxia initially increased ventilation as well as phrenic and carotid sinus nerve activity in anesthetized cats (288 +/- 31, 269 +/- 31, 273 +/- 29% of control value, respectively). During the roll off, ventilation and phrenic nerve activity decreased similarly (to 230 +/- 26 and 222 +/- 28%, respectively after the roll off), but in contrast carotid sinus nerve activity remained unchanged (270 +/- 26%). Thus the ventilatory roll off was reflected in phrenic but not in carotid sinus nerve activity. We conclude that the cat represents a useful animal model of the roll off phenomenon and that the mechanism responsible for the secondary decrease in ventilation lays within the CNS.

摘要

低氧刺激通气,但当低氧持续存在时,通常会出现反应性降低。这种抑制或“衰减”的机制尚不清楚。在本研究中,我们试图将相关机制定位在三个可能的部位之一:颈动脉体、中枢神经系统(CNS)或呼吸装置。对5只清醒和14只麻醉的成年猫进行了对持续低氧(呼气末氧分压,40 - 50托)的通气反应测试。在麻醉和清醒的猫中均发现了衰减现象。在麻醉猫中,等碳酸血症性低氧最初增加了通气以及膈神经和颈动脉窦神经活动(分别为对照值的288±31%、269±31%、273±29%)。在衰减过程中,通气和膈神经活动类似地下降(衰减后分别降至230±26%和222±28%),但相比之下,颈动脉窦神经活动保持不变(270±26%)。因此,通气衰减反映在膈神经活动中,而不是颈动脉窦神经活动中。我们得出结论,猫是衰减现象的一种有用的动物模型,并且通气继发性降低的机制位于中枢神经系统内。

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